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Analyzing breathing irregularities during the post-natal period in spontaneously hypertensive rats


Arterial hypertension (AH) is a cardiovascular disease with a relevant incidence worldwide. Clinical and experimental evidence indicates that increased sympathetic activity to blood vessels primarily contributes to the development of essential AH. Among the factors that can influence the functioning of the sympathetic nervous system is the supply of O2 to the central nervous system (CNS) during the postnatal period. In hypertensive patients and spontaneously hypertensive rats (SH), an experimental model for essential AH, a reduction in the lumen of the vertebrobasilar artery was reported, leading to hypoperfusion and brainstem hypoxia. In SH animals, the condition of central hypoxia is observed from birth, indicating a reduced availability of O2 to the CNS during postnatal development. Studies show that SH animals also exhibit respiratory irregularities with periods of apnea, suggesting changes in the neural network that controls breathing. Such respiratory changes appear to be present from birth and may cause exposure to postnatal intermittent hypoxia. Accordingly, in the present project, we will explore the original hypothesis that SH rats have alterations in the mechanisms of breathing rhythm generation since birth leading to respiratory irregularities and pauses. These changes in breathing in SH rats would result from sensitization of the central mechanisms monitoring tissue O2, present in the ventral surface of the medulla, where the respiratory rhythm generator is located. This O2-sensitive mechanism involves the activation of astrocytes with the release of purines that modulate the activity of rhythmogenic respiratory neurons. Using in vivo approaches to recording ventilation and in vitro electrophysiological protocols, we explore the functioning of the breathing generator and the mechanisms that contribute to the emergence of apneas in hypertensive animals during the postnatal period. (AU)

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